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Effect of exogenous IGF‐1 on chondrocyte apoptosis in a rabbit intraarticular osteotomy model
Author(s) -
Higgins Thomas F.,
Johnson Brian D.
Publication year - 2010
Publication title -
journal of orthopaedic research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.041
H-Index - 155
eISSN - 1554-527X
pISSN - 0736-0266
DOI - 10.1002/jor.20942
Subject(s) - chondrocyte , tunel assay , apoptosis , medicine , in vivo , endocrinology , andrology , cartilage , immunohistochemistry , biology , anatomy , biochemistry , microbiology and biotechnology
Insulin‐like growth factor‐1 (IGF‐1) has been shown to protect chondrocytes from apoptosis in vitro. IGF‐1 expression may also assist in maintaining a fully differentiated chondrocyte phenotype. Theoretically, posttraumatic administration of IGF‐1 may inhibit chondrocyte apoptosis. This study is to determine if administration of IGF‐1 after fracture inhibits apoptosis in vivo. Twenty‐four mature female New Zealand white rabbits were randomized to control and IGF‐1 groups. All subjects underwent standardized medial femoral condyle fracture and repair. Fibrin clot was administered in all subjects, with 25 mcg/ml IGF‐1 in the clot in half the subjects. Half of the animals in each group were sacrificed at 2 weeks and half at 4 weeks, specimens were fixed and underwent TUNEL staining. Two‐week controls showed significantly higher rate of apoptosis than 2‐week IGF‐1 subjects (21 ± 6 vs. 12 ± 6, p = 0.04). Likewise, 4‐week controls showed significantly higher rate of apoptosis than 2‐week IGF‐1 subjects (23 ± 7 vs. 10 ± 2, p = 0.01). There was no significant administration difference between 2‐week control and 4‐week control subjects, or between 2‐week IGF‐1 and 4‐week IGF‐1 subjects. Intraarticular IGF‐1 at the time of fracture repair appears to inhibit chondrocyte apoptosis in vivo, as judged by TUNEL staining, in this animal model. If administration of IGF‐1 inhibits human chondrocyte apoptosis in vivo, this may lead to interventions that may reduce posttraumatic arthritis after fracture. © 2009 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 28:125–130, 2010